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pharmacology unit 6 > antiretrovirals > Flashcards

antiretrovirals Flashcards

1
Q

what are the five classes of antiretrovirals

A

1.) NRTIs. 2.) NNRTIs. 3.) protease inhibitors. 4.) entry inhibitors. 5.) integrase inhibitors

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2
Q

what is the mechanism of the NRTIs

A

they terminate viral DNA chain elongation. inhibition of the reverse transcriptase enzyme.

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3
Q

what kind of molecules are the NRTIs

A

they are nucleoside analogs.

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4
Q

what does zidovudine analog?

A

thymidine

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5
Q

what does stavudine analog

A

thymidine

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6
Q

what does didanosine analog

A

adensosine

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7
Q

what does tenofovir analog

A

adenosine

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8
Q

what does zalcitabine analog

A

cytosine

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9
Q

what does lamivudine analog

A

cytosine

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10
Q

what does emtricitabine analog

A

cytosine

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11
Q

what does abacavir analog

A

guanine

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12
Q

what is the SE of tenofovir

A

nephrotoxicity

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13
Q

what is the SE of abacavir

A

HSR

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14
Q

what are the SE for lamivudine/emtricitabine

A

few

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15
Q

what are the SE for zidovudine

A

anemia

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16
Q

what are the general class SE for NRTIs

A

lactic acidosis and Gi SE

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17
Q

How can the virus become resistant to the NRTIs

A

by mutation. if the virus mutates that base pair enough the drug becomes inactive.

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18
Q

what is the mechanism for NNRTis

A

binds directly to the reverse transcriptase enzyme and inhibits its action. right into the binding pocket.

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19
Q

what are the four common NNRTIs

A

1.) efavirenz, 2.) nevirapine, 3.) etravirine, 4.) rilpivirine

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20
Q

what are the SE for efavirenz

A

CNS symptoms such as vivid dreams, drowsiness. it is also teratogenic.

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21
Q

what are the SE for nevirapine

A

Rash, hepatitis and hepatitis necrosis.

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22
Q

what are the SE for etravirine

A

rash, increased LFTs.

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23
Q

what are the SE for rilpivirine

A

rash and QT prolongation.

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24
Q

what is the mechanism for protease inhibitors

A

binds within the pocket of the protease inhibiting the binding of the virus. without the protease cleavage the virus cannot infect. the polyprotein needs processing

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25
Q

what positive effect does ritonavir have when given in combination with other PI? what is the mechanism?

A

it interacts and increases activity. it inhibits P4503A4 in the liver and gut and also inhibits P-glycoprotein transport.

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26
Q

what is the rationale behond giving ritonavir

A

reduce the frequency of dosing, improve pill burden, improved ability to suppress strains of resistant virus. improves regimen efficacy.

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27
Q

what are the PI class toxicities

A

GI intolerance -nausea, vomit, diarrhea. metabolic toxicities -dyslipidemia, hyperglycemia, lipodystrophy.

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28
Q

what is the mechanism of enfuvirtide

A

inhibits the entry of the virus. binds to GP41 and inhibits the formation of the entry pore, so the virus cannot enter the cell.

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29
Q

what are the SE of enfuvirtide

A

local injection site reaction (pain, erythema, nodules, cysts), increased rate of bacterial pneumonia, HSR (rare)

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30
Q

what is maraviroc?

A

CCR5 antagonist. chemokine receptor inhibitor. this is a coreceptor that is necessary for infection.

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31
Q

what are the SE maraviroc

A

hepatotoxicity rare. cough, fever, URI, rash, MSK, abdominal pain, dizziness.

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32
Q

what are the three integrase inhibitors

A

raltegravir, elvitegravir, dolutegravir

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33
Q

what are the adverse effects of the integrase inhibitors?

A

few. nausea, HA, diarrhea, pyrexia, myopathy or rhabdomyolysis.

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34
Q

what do the integrase inhibitors do?

A

they inhibit the integration of viral DNA into the host genome

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35
Q

what is the recommendation for antiretroviral treatment

A

recommended for all HIV infected patients to reduce the risk of progression. also based on the CD4 count.

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36
Q

what should patients starting ART be willing to do?

A

commit to long-term treatment

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37
Q

what is HAART

A

highly active antiretroviral therapy.

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38
Q

what are the basics of HAART

A

combination therapy of at least 3 active agents. utilization of multiple classes. there are typically three agents that represent 2 classes of agents. this is combination therapy or cocktail therapy.

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39
Q

what are common HAART regimens

A

PI (with ritonavir boost) + 2 NRTIs, NNRTI + 2 NRTIs, integrase inhibitors + 2 NRTIs

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40
Q

what is the recommended NNRTI based HAART

A

efavirenz + (lamivudine or emtricitabine) + tenofovir

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41
Q

what is the recommended PI-based HAART

A

atazanavir/ritonavir or darunavir/ritonavir + (lamivudine or emtricitabine) + tenofovir

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42
Q

what is the integrase-based recommended HAART

A

raltegravir/elvitegravir/dolutegravir + (lamivudine or emtricitabine) + tenofovir

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43
Q

what are the goals of HAART

A

suppression of viral load, restoration of immune function, quality of life, reduce morbidity mortality, minimize risk for resistance.

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44
Q

therapy goals for HAART

A

undetectable viral load <20 within the first 24-48 weeks of therapy. increased CD4 count (this trails the viral load).

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45
Q

what should be done if the patient does not reach the HAART goals

A

change treatment.

46
Q

if resistance is acquired by the HIV is it permanent

A

yes.

47
Q

can cross-resistance occur with antiretroviral treatment

A

yes.

48
Q

what is resistance to HAART atrtributable to?

A

adherence and attainment of goals.

49
Q

how do we monitor the success of HIV treatment

A

viral load, CD4 count, side effects

50
Q

what is the family for HCV

A

flavivirdae.

51
Q

what is the genome for HCV

A

ssRNA with 7 genotypes.

52
Q

how is HCV transmitted>

A

percutaneous, permucosal route. IV drugs, medical supplies, tattoos.

53
Q

is there an effective vaccine for HCV

A

no.

54
Q

is HCV curable

A

yes, with effective treatment

55
Q

what is the mechanism for interferon

A

induces genes that establish an antiviral state within the cell. usually pegylated

56
Q

what are the concerns for interferon treatment

A

not viral specific. flu-like illness, cytopenias, depression, fatigue, difficult treatment course. there are many patietns with contraindications.

57
Q

what are the contraindications for interferon

A

baseline cytopenia or psychiatric problems.

58
Q

what is ribavirin

A

nucleoside analog

59
Q

what are the major SE for ribavirin

A

hemolytic anemia and teratogen.

60
Q

what are the new classes for treatment of HCV

A

nucleotide/side NS5B polymerase inhibitors, NS5A inhibitors, NS3/4A protease inhibitors.

61
Q

what class is sofosbuvir

A

NS5B inhibitor -a nucleoside/tide polymerase inhibitor.

62
Q

what is the class for ledipasvir?

A

NS5A inhibitor.

63
Q

what is the class for simeprevir?

A

NS3/4A protease inhibitor.

64
Q

what is the class for telapevir?

A

NS3/4A protease inhibitor.

65
Q

what is the class for boceprevir

A

NS3/4A protease inhibitor.

66
Q

what is the mechanism for sofosbuvir?

A

inhibits NS5B polymerase of HCV. this is an RNA-dependent RNA polymerase. it becomes phosphorylated and competes with viral uridine (natural) to cause chain termination. a

67
Q

is sofosbuvir active across all HCV genotypes?

A

yes.

68
Q

what are the toxicity for sofosbuvir

A

relatively safe. fatigue, HA, GI SE, anemia possible.

69
Q

what is the mechanism for ledipasvir

A

inhibits viral NS5A a phophoprotein required for replication.

70
Q

what are the toxicities for ledipasvir

A

relatively safe. fatigue, HA, GI SE possible.

71
Q

what is the mechanism of action for simeprevir?

A

prevents viral maturation through inhibition of protein synthesis.

72
Q

what is the mechanism for boceprevir

A

prevention of viral maturation through inhibition of protein synthesis.

73
Q

what is the mechanism for telaprevir

A

prevention of viral maturation through inhibition of protein synthesis.

74
Q

what is the class for the “previr”

A

these are the NS3/4A protease inhibitors.

75
Q

what is the mechanism for all “previr”

A

prevention of viral maturation through inhibition of protein synthesis.

76
Q

what are the SE for “previr”

A

anemia, rash, GI side effects, drug interactiond

77
Q

what do we think when we hear protease inhibitors for viral therapy

A

drug interactions.

78
Q

what is the approach to HCV therapy

A

combination is standard

79
Q

what is the goal of HCV response

A

sustained virologic response or undetected RNA 12-24 weeks after therapy.

80
Q

what is SVR synonymous with in HCV treatment?

A

cure.

81
Q

do we use combination therapy for HCV and how many drugs is typical if yes?

A

yes. more than 2, with multiple mechanisms of action.

82
Q

what is the mechanism of action for the guanosine nucleoside antivirals?

A

activated upon phosphorylation, which requires a cell infected with Herpesvirdae and is expressing thymidine kinase. inhibition of replication of the viral DNA.

83
Q

what is the mechanism for acyclovir

A

phosphorylation by cellular enzymes and thus competes with DAN analogues to cause viral chain termination

84
Q

what is acyclovir primarily active against

A

HSV and VZV

85
Q

what is valacyclovir

A

prodrug of acyclovir that is converted upon oral administration.

86
Q

what is penciclovir

A

structure and MOA similar to acyclovir. often topical.

87
Q

what is famciclovir

A

prodrug of penciclovir given orally.

88
Q

what are the toxicities for acyclovir

A

CNS -malaise, HA, confusion. nausea/vomit, diarrhea, renal dysfunction caused by high doses that crystalize in kidney’

89
Q

what is ganciclovir used for

A

HSV, VZV, CMV.

90
Q

is acyclovir used for CMV?

A

no. inactive against CMV

91
Q

what are the adverse effects for ganciclovir

A

myelosuppression (neutropenia need to monitor), CNS (seizures, confusion, HA). hepatotoxic and some GI intolerance.

92
Q

how can we increased the bioavailability of ganciclovir?

A

take with food increase 6-9%

93
Q

foscarnet is active against which viruses

A

herpesvirdae and HIV.

94
Q

what is the mechanism of action for foscarnet

A

direct inhibition of herpes DNA polymerase or HIV reverse transcriptase.

95
Q

what are useful things to know about foscarnet

A

does not undergo significant cellular metabolism, and is active against acyclovir/penciclovir/ganciclovir resistant viruses.

96
Q

what is an issue with foscarnet?

A

safety. nephrotoxicity. electrolyte/metabolic disorders (calcemia/phophatemia/hypomagnesemia/hypokalemia. CNS side effects (tremor, irritability, seizures, hallucinosis). myelosuppression.

97
Q

what is the treatment of choice for herpes?

A

acyclovir

98
Q

what is the treatment of choice for CMV

A

ganciclovir.

99
Q

which antiviral is used for resistant viruses

A

foscarnet

100
Q

what is the best treatment for influenza

A

vaccination

101
Q

when do we use influenza treatment other than vaccinations

A

when caught early, if it moderately limits the length of illness, there is some benefit for critically ill patients.

102
Q

what is the class for oseltamivir and zanamivir

A

neuraminidase inhibitors.

103
Q

what is the mechanism for oseltamivir and zanamivir

A

inhibit neuraminidase and stops the penetration of the virus into the respiratory system.

104
Q

what strain of flu are the neuraminidase inhibitors good for?

A

both A and B

105
Q

what are the benefits of using the neuraminidase inhibitors

A

there is 30% more rapid resolution of symptoms. significantly reduces the rates of complication (bronchitis. pneumonia). generally well tolerated

106
Q

when do we have to start neuraminidase inhibitors

A

the first 48 hours of symptoms and continue for 5 days.

107
Q

what are the SE of the neuraminidase ihibitors

A

GI (nausea/vomiting/diarrhea), neuropsychiatric events (anxiety, agitation, altered mental status)

108
Q

what are the unique SE of zanamavir

A

since it is inhaled there could be bronchospasms.

109
Q

when do we use chemoprophylaxis for flu

A

througout flu season and post-exposure for a short periofd.

110
Q

who gets chemoprophylaxis for flu

A

high risk and vaccinations were given post exposure, unvaccinated who provide care for high risk, immune deficiency and dont respond to vaccinations, influenza outbreak, any unvaccinated who wishes to avoid.

pharmacology unit 6 (45 decks)

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